Title
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Modification of hormonal secretion in clinically silent pituitary adenomas
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Author
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Abstract
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Background Silent pituitary adenomas are a subtype of adenomas characterized by positive immunoreactivity for one or more hormones classically secreted by normal pituitary cells but without clinical expression, although in some occasions enhanced or changed secretory activity can develop over time. Silent corticotroph adenomas are the classical example of this phenomenon. Patients and Methods A series of about 500 pituitary adenomas seen over a period of 20 years were screened for modification in hormonal secretion. Biochemical and immunohistochemical data were reviewed. Results Two cases were retrieved, one silent somatotroph adenoma and one thyrotroph adenoma, both without specific clinical features or biochemical abnormalities, which presented 20 years after initial surgery with evidence of acromegaly and hyperthyroidism, respectively. While the acromegaly was controlled by a combination of somatostatin analogs and growth hormone (GH) receptor antagonist therapy, neurosurgery was necessary to manage the thyrotroph adenoma. Immunohistochemical examination demonstrated an increase in the number of thyroid stimulating hormone (TSH)-immunoreactive cells compared to the first tissue. Apparently, the mechanisms responsible for the secretory modifications are different, being a change in secretory capacity in the silent somatotroph adenoma and a quantitative change in the silent thyrotroph adenoma. Conclusions These two cases, one somatotroph and one thyrotroph adenoma, are an illustration that clinically silent pituitary adenomas may in rare circumstances evolve over time and become active, as previously demonstrated in silent corticotroph adenomas. |
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Language
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English
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Source (journal)
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Pituitary / Pituitary Society. - Dordrecht, 1998, currens
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Publication
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Dordrecht
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Academic Publishers
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2009
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ISSN
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1386-341X
[print]
1573-7403
[online]
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DOI
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10.1007/S11102-008-0085-7
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Volume/pages
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12
:1
(2009)
, p. 80-86
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ISI
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000262684200013
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Full text (Publisher's DOI)
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